Lectures 13&14: Pathogenicity of Microorganisms Flashcards Preview

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Flashcards in Lectures 13&14: Pathogenicity of Microorganisms Deck (77):
1

Parasites are organisms that 

  • Live on or within a host organism and are metabolically dependent on the host
  • are any organism that cause disease

2

The host is 

larger organism that supports the survival and growth of a smaller organism 

3

Infection

  • A parasite growing and multiplying within/on a host
  • may or may not result in overt infectious disease 

4

Pathogen

  • Any parasite organism causing infectious disease

5

Primary (frank) pathogen

Causes disease by direct interaction with healthy host

6

Opportunistic pathogen

May be part of normal flora and causes disease when it has gained access to other tissue sites or host is immunocomprimised 

7

Pathogenicity

ability to cause disease

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Chain of events for a successful infection 

  • agent identitiy
  • virulence of agent
  • means of exposure to agent
  • dose of agent
  • susceptibility of host to agen 

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infections passed from animal to human are termed

zoonoses

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What does animate mean

from other humans or animals 

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what does inanimate mean

from water, soil, and food

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Natural enviromental location in which the pathogen resides 

Reservoir (can be animate or inanimate)

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organisms that spread disease from one host to another 

vector 

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infectious disease

infection with viruses, bacteria, fungi, protozoa, and helminths

15

Objective changes in body that can be directly observed

Signs

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subjective changes experienced by patient 

symptoms 

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Set of characteristic signs and symtpoms 

disease syndrome

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Incubation period 

period after pathogen entry, before signs and symptoms 

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Prodromal stage

  • Onset of signs and symptoms 
  • not clear enough for diagnosis

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Period of illness

  • disease is most severe, signs and symptoms

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Convalescence

Signs and symptoms begin to disappear

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Course of infectious disease

  • Incubation period
  • Prodromal stage 
  • Period of illness
  • Convalescence

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A pathogen must contact a host and survive within it to cause a disease. To survive, it needs 

  • A suitable environment
  • A source of nutrients
    • in competition with eukaryotic host cells
  • Protection from harmful elements
    • virulence factors allow a pathogen to oucompete host cells and resist their defenses 

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Some survival strategies for pathogens once in the host are

  • Adhesins
  • Enzymes
  • Toxins
  • Invasins
  • Autoinducers

25

Virulence factors determine the 

degree to which a pathogen causes damage, invasion, infectivity 

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What is virulence

degree or intensity of pathogenicity

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Virulence is determined in part by pathogen's ability to 

  • survive outside of host 
    • more dependent on host (cannot survive outside of host)= less virulent
    •  

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What does pathogenicity islands mean

  • Major virulence factors on large segments on chromosomal or plasmid DNA
    • Increase bacterial virulence
    • absent in nonpathogenic members
    • common sequence characteristics
      • insertion-like seqquences for mobility 
      • G + C content different from bacterial genome
      • several open reading frames
    • Can be spread through horizontal transfer of virulence genes to bacteria 

29

What is the first step in disease 

  • entrance and attachment
    • Portal of entry
      • Skin, respiratory, gastrointestinal, urogenital systems, or conjunctiva of eye, parental route (break in barrier defenses)
      • Vector borne, sexual contact, blood transfusion, or organ transplant
    • Adherence 
      • medated by special molecules called adhesins
    • Colonization
      • A site of microbial reproduction on or within host
      • does not necessarily result in tissue invasion or damage 

30

What are the adherence structures of microbes

  • Pili or fimbriae (adhesion molecules on bacterium's cell surface) bind complementary receptor sies on host cell surface

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what is microbial colonization site

  • Site of microbial reporduction on/in host
  • does not necessarily result in tissue damage

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  • Adhesin/ligans bind to receptors on host cells
    • examples on 
      • Streptococcus mutans
      • Escherichia coli
      • Streptococcus pyogenes

 

  • Streptococcus mutans: Glycocalyx
  • Escherichia coli: Fimbriae
  • Streptococcus pyogenes: M protein 

33

Examples of microbial attachment mechanisms in Eschericia coli 

  • Type I fimbrae ( leads to diarrhea and UTI)
  • P pili (leads to Hemolytic uremic syndrome)

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Adhesion mechanism of Streptococcus pyogenes

  • Protein F (causes strep throat)

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Attachement mechanism of streptococcus mutans

sugar residue/glycocalyx (causes dental caries) 

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Infectivity 

ability to create a discrete point of infection 

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invasiveness

ability to spread to adjacent tissues 

38

Penetration can be active or passive explain both

  • active occurs through lytic substances which
    • attack the extracellular matrix and basement membranes of integuments and intestinal linings
    • degrade carbohydrate-protein complexes between cells
    • disrupts host cell surface
  • passive (e.g. Skin lesions, insect bites, wounds)
    • spread to deeper tissues involves production of specific products and/or enzymes that promote spreading 

39

Virulence factor produced by Staphylococcus aureus for bacterial pathogen invasion and dissemination

Coagulase: Coagulates (clots) the fibrinogen in plasma/ The clot protects the pathogen from phagocytosis and isolates it from other host defenses. 

40

Virulence factor produced by Groups A,B,C, and G streptococci, staphylococci, clostridia for bacterial pathogen invasion and dissemination

Hyaluronidase: hydrolyzes hyaluronic acid, a constituent of the extacellular matrix that cements cells together and render the intercellular spaces amenable to passage by the pathogen 

41

Virulence factor produced by Staphylococci, pneumonocci, and other streptococci for bacterial pathogen invasion and dissemination

Leukocidins: pore-forming exotoxins that kill leukocytes; cause degranulation of lysosomes within leukocytes, which decrease host resistance 

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presence of viable bacteria in the blood 

bacteremia

 

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Pathogens or their toxins in the blood 

septicemia 

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Invasiveness varies among pathogens. Examples 

  • Clostridium tetani (tetanus) produces a number of virulence factors but is non-invasive
  • Bacillus anthracis (anthrax) and Yersinia pestis (plague) also produce many virulence factors and are highly invasive
  • Streptococcus spp. span the spectrum of virulence factors and invasiveness 

45

what is toxigenicity

ability to produce toxins

 

46

What is a toxin

a specific substance that damages host 

47

Diseases that result from entry of a specific preformed toxin into host (Ex. Tetanus toxin)

Intoxications

48

Toxemia 

condition caused by toxins in the blood of host

49

Exotoxins

  • Soluble, heat-labile, proteins
  • secreted into surroundings as pathogen grows
  • most exotoxin producers are gram-positive
  • often travel form site of infection to other tissues or cells where they exert their effects
  • Usually synthesized by specific bacteria that have toxin genes in their plasmids or prophage DNA
  • Among the most lethal substances known
  • Are highly immunogenic
  • Stimulate production of neutralizing Ab (antitoxins)
  • Chemically inactivated to form immunogenic toxoids
    • e.g. Tetanus toxoid
  • do not produce a fever (but they are heat labile) 
  • LD50 is small 

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Types of Exotoxins

  • AB exotoxins
    • Composed of two subunits
      • A subunit- responsible for toxic effect
      • B subunit- binds to specific target cell
  • Specific host site exotoxins
  • Membrane-disrupting exotoxins
  • Superantigens 

52

Botulinum toxin

  • Organism:
    • Clostridium botulinum
  • Gene location:
    • Prophage
  • Toxin type:
    • AB
  • Mechanism of Action: 
    • Blocks neurotransmitter release, leading to paralysis  (flaccid paralysis) 
    • specificially it attacks SNAP25 and Syntaxin and does not allow the Ach to be moved to the synaptic terminal and released into the synaptic cleft 

53

Tetanospasmin

  • Organism:
    • Clostridium tetani
  • Gene location: 
    • Plasmid
  • Toxin type:
    • AB
  • Mechanism of Action
    • Blocks neurotransmitter, leadin to spastic paralysis 
    • proteolysis of Synaptobrevin

54

Superantigens

 

  • Stimulate about 30% of T cells of the immune system
    • Causes the T cells to overexpress and release cytokines
    • results in failure of multiple host organs allowing time for the microbe to disseminate
  • Example 
    • Staphylococcal enterotoxin B

55

Endotoxins

  • Lipopolysaccharide (LPS) in Gram-negative cell wall can be toxic to specific hosts
    • called endotoxin because it is an endogenous (part) of the bacterium and released when organism lyses
      • some is also released during multiplication
    • Toxic component is the lipid portion, lipid A
  • Heat Stable (but do produce fever)
  • Toxic (nanogram amounts)
  • Weakly immunogenic 
  • Generally similar, despite source
  • Cause general system effects
    • Fever, weakness, diarrhea, inflammation, intestinal hemorrhage, and fibrinolysis, the enzymatic breakdown of fibrin, the major protein component of blood clots
    • Bring about these effects indirectly:
      • endotoxin interacts with host molecules and cells, activating host systems
        • coagulation, complement, fibrinolytic, and kininogen system
      • e.g. interaction with macrophages---> release of endogenous pyrogen (induces fever) 
      • e.g. binding to LPS-binding protein ---> release of cytokines
        • tumor necrosis and others lead to septic shock
  • LD50 is relatively large
  • chemistry: 
    • lipid
  • Source:
    • Gram-negative 
  • Not neutralized by antitoxin

56

Mycotoxins

  • Secondary metabolites of fungi
    • common contaminants of food crops
    • Aspergillus flavus and A. parasiticus produce carcinogenic aflatoxin
    • Stachybotrys produce tissue-damaging satratoxins
    • Claviceps purpurea (ergot) produce hallucinogen lysergic acid (LSD)

57

effects of pathogen biofilm growth

  • May cause a chronic infection
  • increases virulence
  • become less sensitive to antibiotics
  • make cells in biofilm more resistant to host defense ("frustrates" phagocytes) 

58

Cell wall components of pathogens that are increase virulence

  • M protein resists phagocytosis 
    • ex. Streptococcus pyogenes
  • Opa protein inhibits T helper cells
    • Ex. Neisseria gonorrhoeae
  • Mycolic acid (Waxy lipid) resists digestion
    • Ex. Mycobacterium tuberculosis

59

Resisting host defenses  

  • Production of decoy proteins to bind available neutralizing antibodies
  • Lengthened O-chains to prevent host detection or lysis
  • some survive inside host cells
    • eject themselves form cell to cell using host actin
    • ex. Shigella sp. and Rickettsia sp. 
  • Infection of immune system cells, diminishing function
  • Fuse with adjacent cells to prevent exposure to antimicrobial proteins in host
  • Capsules prevent phagocytosis 
  • Mutations change antigenic sites or alter expression of antigens
    • thourhg downregulation or phase variation (ex. Altered Pilin protein, N. gonorrhea) 
  • Produce substances that resemble host tissue
  • Produce proteases that degrade host proteins
  • Special proteins that interfere with host defenses

60

Examples of Capsules and function

  • Prevent phagocytosis 
    • Streptococcus pneumoniae
    • Haemophilus influenzae
    • Bacillus anthracis
    • Staphylococcus aureus 

61

Pathogen Enzymes

  • Coagulase
    • Coagulates fibrinogen
  • Kinases
    • Digest fibrin clots
  • Hyaluronidase
    • Hydrolyzes hyaluronic acid (found in CT)
  • Collagenase
    • Hydrolyzes collagen
  • IgA proteases
    • Destroy IgA antibodies 

62

Evidence suggests correlation between mode of transmission and degree of virulence

  • Direct contact
    • less virulent
  • Vector-borne
    • highly virulent in human host; relatively benign in vector
  • Greater ability to survive ouside host 
    • means more virulent

63

What is Tropism

  • Tropism
    • Pathogen must make contact with appropriate host tissue
      • determined by specific cell surface receptors 
  • (note that transmission alone is not enough for infection to occur) 

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What are the five main modes of transmission

  • Airborne (indirect)
  • contact 
  • vehicle (indirect)
  • vector borne 
  • vertical 

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inanimate materials or objects involved in pathogen transmission

Vehicles

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Fomites

Common vehicle such as surgical instruments, bedding, and eating utensils

69

What is the difference between harborage transmission and biological transmission

  • Both are types of internal transmission for vector-borne transmission
  • Harborage transmission
    • pathogen does not undergo changes within vector
  • Biologic transmission
    • pathogen undergoes changes within vector 

70

Occurss when the unborn child aquires a pathogen form an infected mother

Vertical transmission 

71

Examples of congential infection (born with infection)

  • gonorrhea (especially in the eyes)
  • herpes
  • german measles
  • toxoplasmosis 

72

What is infectious dose 50

Dose that causes 50% of the host organisms to become infected

73

Infectious dose 50 for Bacillus anthracis in each of the 3 portals of entry

  • ID50 through skin:
    • is 10-50 endospores
  • ID50 through inhalation: 
    • is 10,000 to 20,000 endospores
  • ID50 through GI is 250,000-1,000,000 endospores 

74

Cytopathology

  • Can be used to observe cells in tissue culture for death rates rather than entire organisms 

75

What are the two main factors of host susceptibility

  • Defense mechanisms of host (innate and adapted/acquired immunity)
  • Pathogenicity of pathogen
  • (note that nutrition, genetic predisposition, and stress also play a role in host susceptibility to infection) 

76

What are the portals of exit for a pathogen

  • Respiratory tract
    • coughing and sneezing
  • Gastrointestinal tract 
    • Feces and saliva
  • Genitourinary tract
    • urine and vaginal secretions
  • Skin
  • Blood
    • biting arthropods and needles or syringes

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